JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2017, Vol. 55 ›› Issue (10): 65-70.doi: 10.6040/j.issn.1671-7554.0.2016.1152

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Perindopril ameliorates cardiac dysfunction via Akt-FoxO1 pathway in diabetic cardiomyopathy

GONG Luwei, ZHOU Lizhen, SU Guohai   

  1. Department of Cardiology, Jinan Central Hospital, Affiliated to Shandong University, Jinan 250013, Shandong, China
  • Received:2016-09-13 Online:2017-10-10 Published:2017-10-10

Abstract: Objective To investigate the role and potential mechanism of perindopril on myocardial dysfunction in DCM(diabetic cardiomyopathy). Methods A total of 40 male Sprague-Dawley rats(100-120 g)were divided into 3 groups: control(n=10), DCM group(n=15)and DCM+perindopril group(n=15). The control group was fed with basal diet, while the DCM group and DCM+perindopril group were established as diabetic models. After the models were successfully established, the DCM group received intragastric normal saline, and DCM+perindopril group received intragastric perindopril 4 mg/(kg·d). The effect of perindopril on the rats cardiac function, myocardial apoptosis and fibrosis were observed. The protein expressions of p-Akt and p-FoxO1 were examined withWestern blotting. Results Compared with the control group, the DCM group exhibited severe left ventricular dysfunction, myocardial apoptosis and fibrosis, significantly increased p-FoxO1 expressio and decreased p-Akt protein expression(P<0.05). Compared with the DCM group, the DCM+perindopril group had better cardiac function and lower p-Akt protein expression(P<0.05). Conclusion Perindopril protects cardiac function by inhibiting myocardial apoptosis and fibrosis in diabetic rat svia Akt-FoxO1 pathway.

Key words: Perindopril, Cardiac function, Apoptosis, Fibrosis, Diabetic cardiomyopathy

CLC Number: 

  • R587.2
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